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Int Neurourol J > Volume 10(2); 2006 > Article
Fundamental Science for Neurourology
Journal of the Korean Continence Society 2006;10(2): 132-139.
DOI: https://doi.org/10.5213/jkcs.2006.10.2.132   
Apoptosis Induction and Clusterin Expression of NRP-152 Cells by Tamsulosin.
Yun Hee Youm, Yong Dal Yoon, Jea Hyung Woo, Tag Keun Yoo
1Department of Urology and Life Science Institute, Eulji University School of Medicine, Korea. ytk5202@eulji.or.kr
2Department of Life Science, Hanyang University, Seoul, Korea.
ABSTRACT
PURPOSE
The aim of this study was to know whether and how tamsulosin induces apoptosis of normal rat prostate cells, and the relationship between apoptosis and clusterin expression.
MATERIALS AND METHODS
We used a prostate cell line, NRP-152 cells which are the basal epithelium cell originated from rat prostate. The NRP-152 cells were treated with various concentrations(50, 100, 200, 400 uM) of tamsulosin for 24 h. To evaluate apoptosis, the cultured NRP-152 cells were stained with Heochst 33258 and Propidium Iodide (PI) without fixation. We also examined DNA fragmentation analysis to confirm apoptosis. In addition, to elucidate the signal transduction pathway by which apoptosis is induced, we examined Bcl-2 family proteins such as Bcl-2, Bax, Bad, Bcl-xL, and Bim by real-time RT-PCR.
RESULTS
After tamsulosin treatment, the rate of apoptosis was 25% at 100 micrometer, 50% at 200 micrometer, and 63% at 400 micrometer, whereas the rate of necrosis was 10% at 100 micrometer, 38% at 200 micrometer, and 56% at 400 micrometer. DNA fragmentation was also gradually increased and the highest at 400 micrometer, similar to apoptotic cell rates. As a result of real-time RT-PCR, there was significant difference of Bcl-2 and Bim mRNA expression among the groups. Expression of clusterin protein was significantly increased after treatment of tamsulosin, even as low as 50 micrometer concentration.
CONCLUSION
These results demonstrate that tamsulosin causes the cell death of NRP-152 cells, displaying low concentration of tamsulosin induces apoptosis, but high concentration occurs necrosis. Bim, a proapoptotic factor of the Bcl-2 family, expression was increased in the cells treated with tamsulosin, whereas Bcl-2 expression was decreased. The present study suggests that clusterin may play a role in the process of apoptosis induced by tamsulosin and Bim could be involved in the apoptosis.
Keywords: Apoptosis; Clusterin; Prostate cells; Tamsulosin
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Official Journal of Korean Continence Society & ESSIC (International Society for the Study of BPS) & Korean Society of Urological Research & The Korean Children’s Continence and Enuresis Society & The Korean Association of Urogenital Tract Infection and Inflammation & Korean Society of Geriatric Urological Care
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